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A 2016 study implicated the C4A gene in schizophrenia risk. C4A was found to play a role in synaptic pruning, and increased C4A expression leads to reduced dendritic spines and a higher schizophrenia risk. [36]
Loss-of-function mutations at the gene encoding histone H3 methyltransferase, an important enzyme for epigenetic histone modification, have also been implicated in gene-association studies for schizophrenia. [13] Histone modification is not the only epigenetic mechanism thought to be commonly associated with schizophrenia.
Other studies have implicated that a loss-of-function translocation mutation in the DISC1 gene is a major risk factor in developing schizophrenia. The DISC1 gene codes for a scaffold protein that assists with neurite outgrowth and development of the cortex, operating at several intersections of neurodevelopmental pathways. [27]
Disrupted in schizophrenia 1 is a protein that in humans is encoded by the DISC1 gene. [5] In coordination with a wide array of interacting partners, DISC1 has been shown to participate in the regulation of cell proliferation, differentiation, migration, neuronal axon and dendrite outgrowth, mitochondrial transport, fission and/or fusion, and cell-to-cell adhesion.
Estimates of the heritability of schizophrenia are between 70% and 80%, which implies that 70% to 80% of the individual differences in risk of schizophrenia are associated with genetics. [ 21 ] [ 84 ] These estimates vary because of the difficulty in separating genetic and environmental influences, and their accuracy has been queried.
The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors .
If possible to test for schizophrenia before the symptoms develop, proactive interventions could be developed, or even preventative treatments. [7] In one study, 100% of patients with bipolar disorder indicated that they would probably take a genetic test to determine they were carrying a gene associated with the disorder, if such a test ...
UHMK1 also phosphorylates the CNS proteins myelin basic protein (MBP) and synapsin I so that genetic abnormalities in UHMK1 could contribute to the genetic cause of schizophrenia through several different brain pathways. UHMK1 is also implicated in the progression of many cancers such as gastric, [11] liver, [12] colorectal, [13] cervical [14 ...
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